There is a great deal of evidence from computerized tomography (CT) that the lungs of patients with acute respiratory distress syndrome (ARDS) are inhomogeneously affected. The aim of this proposal is to measure the distribution of regional volume expansion in injured lungs and to study the effects of positive end-expiratory pressure, frequency, alveolar flooding, and antifoaming agents on these distributions. The regional distribution of lung expansion will be measured in oleic acid injured anesthetized dogs using the parenchymal marker technique. Regional edema and its redistribution during mechanical ventilation will be measured using CT technology. Our motivation is the absence of experimental data on the regional dynamics of injured lungs. Without such data, mechanical ventilation strategies that are to protect aerated lung from overdistension yet promote recruitment of flooded or collapsed units must be based on untested assumptions. The classic model of Otis and Mead suggests that inhomogeneity promotes frequency-dependent behavior. However, this inherently linear model remains to be validated in biologic systems and it may not be appropriate for analyzing the mechanical behavior of injured lungs. CT technology, which has shaped many current hypotheses in the field, has a limited temporal and spatial resolution and cannot discern the displacements of specific structures in the lung from which to compute regional volume and deformation. This is the gap in knowledge that our proposal intends to fill. Accepted models of regional mechanics in, ARDS view dependent lung units as compressed by the weight of overlying edematous tissue. Our preliminary data suggest otherwise. The volume of dependent lung is increased, not reduced, implying a different mechanism. Modeling and engineering analyses will be used to interpret the data and to test hypotheses about the effects of tissue impedance and airway impedance on the distribution of regional lung expansion.